Gallant P E
Laboratory of Neurobiology, National Institute of Neurological Disease and Stroke, National Institutes of Health, Bethesda, Maryland 20890.
J Neuropathol Exp Neurol. 1992 Mar;51(2):220-30. doi: 10.1097/00005072-199203000-00011.
The direct effects of mechanical compression on axoplasm and fast axoplasmic transport were studied by video-enhanced differential interference microscopy. Single axons, isolated from the squid, were compressed with 0.5, 5, 20, or 100 gram (g) weights placed over a 1 millimeter (mm) length of axon. Brief compressions (10 seconds) at low pressures (0.5 g/mm) momentarily deformed the axon, but the axoplasm and axon returned to their normal shape and position after the pressure was removed, and no residual changes in axoplasmic structures, fast axoplasmic transport or membrane function were seen. Compressing the axon with 5-20 g/mm, however, broke the axoplasm at the site of the crush and squeezed the axoplasm out from under the compression site. Though the axoplasm usually returned to the crush site after the weight was removed and organelles continued to move in the axoplasm under the crush, the organelles failed to cross a dense line that marked the site of the rejoined axoplasm, instead they accumulated over time at the crush site. This results suggests that the blockage of fast transport at moderate compressions was due to a mechanical breakage of the axoplasm at the compression site. The plasma membrane was apparently not transected after moderate compressions (5-20 g/mm) since the resting membrane potential returned to nearly control levels after the weight was removed. Compressions with 100 g/mm, however, did break the plasma membrane as evidenced by the rapid and irreversible loss of the action potential and resting potential and the ion-dependent liquefaction of axoplasm and loss of all organelle transport at the 100 g/mm compression site. Thus, small mechanical pressure elastically deformed the axoplasm, moderate pressures mechanically broke the axoplasm, and high pressures broke the axoplasm and the plasma membrane.
通过视频增强微分干涉显微镜研究了机械压缩对轴浆和快速轴浆运输的直接影响。从鱿鱼分离出的单个轴突，在1毫米长的轴突上放置0.5克、5克、20克或100克重物进行压缩。在低压（0.5克/毫米）下短暂压缩（10秒）会使轴突瞬间变形，但压力去除后轴浆和轴突会恢复到正常形状和位置，且未观察到轴浆结构、快速轴浆运输或膜功能的残留变化。然而，用5 - 20克/毫米压缩轴突时，在挤压部位轴浆会断裂，并从挤压部位下方挤出轴浆。虽然重物移除后轴浆通常会回到挤压部位，细胞器在挤压部位下方的轴浆中继续移动，但细胞器无法穿过标记重新连接轴浆部位的致密线，而是随着时间在挤压部位积累。这一结果表明，中等压缩时快速运输的阻断是由于挤压部位轴浆的机械断裂。中等压缩（5 - 20克/毫米）后质膜显然未被横断，因为重物移除后静息膜电位恢复到接近对照水平。然而，100克/毫米的压缩确实会破坏质膜，这可由动作电位和静息电位的快速且不可逆丧失以及在100克/毫米压缩部位轴浆的离子依赖性液化和所有细胞器运输的丧失来证明。因此，小的机械压力使轴浆发生弹性变形，中等压力使轴浆机械断裂，而高压力则使轴浆和质膜断裂。
